Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA198022 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Columnar cell hyperplasia (CCH) is the first histologically identifiable lesion in the breast with premalignant potential. Altered miRNA expression in the stroma surrounding CCH compared to normal tissue was discovered. The effect of upregulation of one specific miRNA was investigated by gene expression array in human mammary fibroblasts as well as in epithelial CCH cells coculterd with miR-132 oversexpressing human mammary fibroblasts. We used microarrays to detail the effects of miR-132 in human mammary fibroblasts and identified multiple altered genes and gene pathways both in the fibroblasts and in cocultured human mammary epithelial CCH cells.
2014-07-15 | GSE46197 | GEO
Project description:Columnar cell hyperplasia (CCH) is the earliest histologically identifiable breast lesion linked to cancer progression and is characterized by increased proliferation, decreased apoptosis and elevated oestrogen receptor a expression. The mechanisms underlying the initiation of these lesions have not been clarified but might involve early and fundamental changes in cancer progression. MiRNAs are key regulators of several biological processes, acting by influencing the posttranscriptional regulation of numerous targets, thus making miRNAs potential candidates in cancer initiation. Here we have defined novel epithelial as well as stromal miRNA signatures from columnar cell hyperplasia lesions compared to normal terminal duct lobular units by using microdissection and miRNA microarrays. MiR-27a, miR-92a and let-7c were among the identified downregulated epithelial miRNAs and their functions were delineated in unique CCH derived cells suggesting pro-apoptotic and anti-proliferative properties for the selected miRNAs and that downregulation of let-7c in CCH cells potentially increased proliferation via Myb. MiR-132 was upregulated in the stroma surrounding CCH compared to stoma surrounding TDLUs, and overexpression of miR-132 in immortalized fibroblasts and in fibroblasts co-cultured with epithelial CCH cells caused substantial expression changes. Global miRNA expression was also examined both epithelial and stroma of one patient displaying TDLU, CCH and additional invasive breast cancer. The miRNA signatures identified in CCH indicate concordant early changes in the epithelial and stromal compartment of CCH and could represent early key alterations in breast cancer progression that potentially could be targeted in novel prevention or treatment schedules.
2014-07-15 | GSE46198 | GEO
Project description:Analysis of differences at gene expression level of hpvE6 immortalized fibroblasts isolated from normal mammary glands and from hyperplasia, adenoma and carcinoma stages using the MMTV-PyMT model (FVB/N background). Analysis demonstrated the activation of specific transcriptional programs in fibroblasts from later stages. Total RNA obtained from isolated hpvE6 immortalized fibroblasts from normal mammary gland (NF) and from different stages of tumour development using the MMTV-PyMT murine breast cancer model. Stages were hyperplasia (HpAF), adenoma (AdAF) and carcinoma (CAF). Fibroblasts were seeded in a deformable Matrigel:collagen I matrix and total RNA isolated 72h later.
2013-03-19 | E-GEOD-45256 | biostudies-arrayexpress
Project description:Mice deficient for miR-212/132 have been reported to show impaired mammary gland development. However, another miR-212/132-deficient line does not demonstrate any obvious defects in mammary gland organogenesis. The transcriptome analysis in the mammary gland of the previously reported miR-212/132-deficient line by deep RNA-seq revealed significantly deregulated expression of genes flanking Mir-212/132 locus, such as HIC1, implying that the mammary gland phenotype might not be only due to loss of miR-212/132
2014-07-29 | GSE37952 | GEO
Project description:Analysis of differences at gene expression level of hpvE6 immortalized fibroblasts isolated from normal mammary glands and from hyperplasia, adenoma and carcinoma stages using the MMTV-PyMT model (FVB/N background). Analysis demonstrated the activation of specific transcriptional programs in fibroblasts from later stages.
2013-03-19 | GSE45256 | GEO
Project description:MiR-132 is one of the most upregulated miRNAs in human skin wounds at the inflammatory phase of healing; however its biological role in dermal fibroblasts during wound repair has not been studied. To study the genes regulated by miR-132, we transfected miR-132 mimics (pre-miR-132) into primary human dermal fibroblasts to overexpress miR-132. We performed a global transcriptome analysis of fibroblasts upon overexpression of miR-132 using Affymetrix arrays.
2016-11-01 | GSE87436 | GEO
Project description:Mice deficient for miR-212/132 have been reported to show impaired mammary gland development. However, another miR-212/132-deficient line does not demonstrate any obvious defects in mammary gland organogenesis. The transcriptome analysis in the mammary gland of the previously reported miR-212/132-deficient line by deep RNA-seq revealed significantly deregulated expression of genes flanking Mir-212/132 locus, such as HIC1, implying that the mammary gland phenotype might not be only due to loss of miR-212/132 Mammary gland mRNA profiles of Wild Type and Mir-212/132ILN/ILN mice were generated by deep sequencing using Illumina GAIIx.
2014-07-29 | E-GEOD-37952 | biostudies-arrayexpress
Project description:Despite some success of pharmacotherapies targeting primarily neurohormonal dysregulation, heart failure is a growing global pandemic with increasing burden. Treatments that improve the disease by reversing heart failure at the cardiomyocyte level are lacking. MicroRNAs (miRNA) are transcriptional regulators of gene expression, acting through complex biological networks, and playing thereby essential roles in disease progression. Adverse structural remodelling of the left ventricle due to myocardial infarction (MI) is a common pathological feature leading to heart failure. We previously demonstrated increased cardiomyocyte expression of the miR-212/132 family during pathological cardiac conditions. Transgenic mice overexpressing the miR-212/132 cluster (miR-212/132-TG) develop pathological cardiac remodelling and die prematurely from progressive HF. Using both knockout and antisense strategies, we have shown miR-132 to be both necessary and sufficient to drive the pathological growth of cardiomyocytes in a murine model of left ventricular pressure overload. Based on the findings, we proposed that miR-132 may serve as a therapeutic target in heart failure therapy. Here we provide novel mechanistic insight and translational evidence for the therapeutic efficacy in small and large animal models (n=135) of heart failure. We demonstrate strong PK/PD relationship, dose-dependent efficacy and high clinical potential of a novel optimized synthetic locked nucleic acid phosphorothioate backbone antisense oligonucleotide inhibitor of miR-132 (antimiR-132) as a next-generation heart failure therapeutic.
2020-01-09 | PXD015337 | Pride
Project description:To examine the effects of recombinant granulin on human mammary stromal fibroblasts, we cultured immortalized GFP+ normal human mammary fibroblasts in the presence of recombinant human granulin (1ug/ml) or PBS every 24h for 6 days. To generate GRN-independent CAFs, we injected immortalized GFP+ human mammary fibroblasts, MCF7Ras human breast carcinoma cells, and 20% Matrigel subcutaneously into nude mice. Tumors were allowed to form for a period of 45 days. GFP+ fibroblasts were isolated from tumors by mincing the tumors, dissociating, and culturing in the presence of 1 ug/ml puromycin for ~3-4 weeks. CAF purity was confirmed by ensuring that 100% of the population was GFP-positive.
2016-07-21 | GSE75333 | GEO